By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer's disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer's and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer's patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered "a strong, independent risk factor for the development of dementia and Alzheimer's disease." Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer's cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don't we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer's disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging--that is, actually seeing what's happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer's disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer's disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer's disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn't it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren't getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don't even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don't eat the minimum recommendation for beans.

If we put people on a healthy diet--a plant-based diet--we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren't getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.

By our seventies, one in five of us will suffer from cognitive impairment. Within five years, half of those cognitively impaired will progress to dementia and death. The earlier we can slow or stop this process, the better.

Although an effective treatment for Alzheimer's disease is unavailable, interventions just to control risk factors could prevent millions of cases. An immense effort has been spent on identifying such risk factors for Alzheimer's and developing treatments to reduce them.

In 1990, a small study of 22 Alzheimer's patients reported high concentrations of homocysteine in their blood. The homocysteine story goes back to 1969 when a Harvard pathologist reported two cases of children, one dating back to 1933, whose brains had turned to mush. They both suffered from extremely rare genetic mutations that led to abnormally high levels of homocysteine in their bodies. Is it possible, he asked, that homocysteine could cause brain damage even in people without genetic defects?

Here we are in the 21st century, and homocysteine is considered "a strong, independent risk factor for the development of dementia and Alzheimer's disease." Having a blood level over 14 (µmol/L) may double our risk. In the Framingham Study, researchers estimate that as many as one in six Alzheimer's cases may be attributable to elevated homocysteine in the blood, which is now thought to play a role in brain damage and cognitive and memory decline. Our body can detoxify homocysteine, though, using three vitamins: folate, vitamin B12, and vitamin B6. So why don't we put them to the test? No matter how many studies find an association between high homocysteinea and cognitive decline, dementia, or Alzheimer's disease, a cause-and-effect role can only be confirmed by interventional studies.

Initially, the results were disappointing. Vitamin supplementation did not seem to work, but the studies were tracking neuropsychological assessments, which are more subjective compared to structural neuroimaging--that is, actually seeing what's happening to the brain. A double-blind randomized controlled trial found that homocysteine-lowering by B vitamins can slow the rate of accelerated brain atrophy in people with mild cognitive impairment. As we age, our brains slowly atrophy, but the shrinking is much accelerated in patients suffering from Alzheimer's disease. An intermediate rate of shrinkage is found in people with mild cognitive impairment. The thinking is if we could slow the rate of brain loss, we may be able to slow the conversion to Alzheimer's disease. Researchers tried giving people B vitamins for two years and found it markedly slowed the rate of brain shrinkage. The rate of atrophy in those with high homocysteine levels was cut in half. A simple, safe treatment can slow the accelerated rate of brain loss.

A follow-up study went further by demonstrating that B-vitamin treatment reduces, by as much as seven-fold, the brain atrophy in the regions specifically vulnerable to the Alzheimer's disease process. You can see the amount of brain atrophy over a two-year period in the placebo group versus the B-vitamin group in my Preventing Brain Loss with B Vitamins? video.

The beneficial effect of B vitamins was confined to those with high homocysteine, indicating a relative deficiency in one of those three vitamins. Wouldn't it be better to not become deficient in the first place? Most people get enough B12 and B6. The reason these folks were stuck at a homocysteine of 11 µmoles per liter is that they probably weren't getting enough folate, which is found concentrated in beans and greens. Ninety-six percent of Americans don't even make the minimum recommended amount of dark green leafy vegetables, which is the same pitiful number who don't eat the minimum recommendation for beans.

If we put people on a healthy diet--a plant-based diet--we can drop their homocysteine levels by 20% in just one week, from around 11 mmoles per liter down to 9 mmoles per liter. The fact that they showed rapid and significant homocysteine lowering without any pills or supplements implies that multiple mechanisms may have been at work. The researchers suggest it may be because of the fiber. Every gram of daily fiber consumption may increase folate levels in the blood nearly 2%, perhaps by boosting vitamin production in the colon by all our friendly gut bacteria. It also could be from the decreased methionine intake.

Methionine is where homocysteine comes from. Homocysteine is a breakdown product of methionine, which comes mostly from animal protein. If we give someone bacon and eggs for breakfast and a steak for dinner, we can get spikes of homocysteine levels in the blood. Thus, decreased methionine intake on a plant-based diet may be another factor contributing to lower, safer homocysteine levels.

The irony is that those who eat plant-based diets long-term, not just at a health spa for a week, have terrible homocysteine levels. Meat-eaters are up at 11 µmoles per liter, but vegetarians at nearly 14 µmoles per liter and vegans at 16 µmoles per liter. Why? The vegetarians and vegans were getting more fiber and folate, but not enough vitamin B12. Most vegans were at risk for suffering from hyperhomocysteinaemia (too much homocysteine in the blood) because most vegans in the study were not supplementing with vitamin B12 or eating vitamin B12-fortified foods, which is critical for anyone eating a plant-based diet. If you take vegans and give them B12, their homocysteine levels can drop down below 5. Why not down to just 11? The reason meat-eaters were stuck up at 11 is presumably because they weren't getting enough folate. Once vegans got enough B12, they could finally fully exploit the benefits of their plant-based diets and come out with the lowest levels of all.

According to the Centers for Disease Control and Prevention, the rates of all of our top 10 killers have fallen or stabilized except for one, suicide. As shown in my video, Antioxidants & Depression, accumulating evidence indicates that free radicals may play important roles in the development of various neuropsychiatric disorders including major depression, a common cause of suicide.

In a study of nearly 300,000 Canadians, for example, greater fruit and vegetable consumption was associated with lower odds of depression, psychological distress, self-reported mood and anxiety disorders and poor perceived mental health. They conclude that since a healthy diet comprised of a high intake of fruits and vegetables is rich in anti-oxidants, it may consequently dampen the detrimental effects of oxidative stress on mental health.

But that study was based on asking how many fruits and veggies people ate. Maybe people were just telling the researchers what they thought they wanted to hear. What if you actually measure the levels of carotenoid phytonutrients in people's bloodstreams? The same relationship is found. Testing nearly 2000 people across the United States, researchers found that a higher total blood carotenoid level was indeed associated with a lower likelihood of elevated depressive symptoms, and there appeared to be a dose-response relationship, meaning the higher the levels, the better people felt.

Lycopene, the red pigment predominantly found in tomatoes (but also present in watermelon, pink grapefruit, guava and papaya) is the most powerful carotenoid antioxidant. In a test tube, it's about 100 times more effective at quenching free radicals than a more familiar antioxidant like vitamin E.

Do people who eat more tomatoes have less depression, then? Apparently so. A study of about a thousand older men and women found that those who ate the most tomato products had only about half the odds of depression. The researchers conclude that a tomato-rich diet may have a beneficial effect on the prevention of depressive symptoms.

Higher consumption of fruits and vegetables has been found to lead to a lower risk of developing depression, but if it's the antioxidants can't we just take an antioxidant pill? No.

Only food sources of antioxidants were protectively associated with depression. Not antioxidants from dietary supplements. Although plant foods and food-derived phytochemicals have been associated with health benefits, antioxidants from dietary supplements appear to be less beneficial and may, in fact, be detrimental to health. This may indicate that the form and delivery of the antioxidants are important. Alternatively, the observed associations may be due not to antioxidants but rather to other dietary factors, such as folate, that also occur in plant-rich diets.

In a study of thousands of middle-aged office workers, eating lots of processed food was found to be a risk factor for at least mild to moderate depression five years later, whereas a whole food pattern was found to be protective. Yes, it could be because of the high content of antioxidants in fruits and vegetables but could also be the folate in greens and beans, as some studies have suggested an increased risk of depression in folks who may not have been eating enough.

Low folate levels in the blood are associated with depression, but since most of the early studies were cross-sectional, meaning a snapshot in time, we didn't know if the low folate led to depression or the depression led to low folate. Maybe when you have the blues you don't want to eat the greens.

But since then a number of cohort studies were published, following people over time. They show that a low dietary intake of folate may indeed be a risk factor for severe depression, as much as a threefold higher risk. Note this is for dietary folate intake, not folic acid supplements; those with higher levels were actually eating healthy foods. If you give people folic acid pills they don't seem to work. This may be because folate is found in dark green leafy vegetables like spinach, whereas folic acid is the oxidized synthetic compound used in food fortification and dietary supplements because it's more shelf-stable. It may have different effects on the body as I previously explored in Can Folic Acid Be Harmful?

These kinds of findings point to the importance of antioxidant food sources rather than dietary supplements. But there was an interesting study giving people high dose vitamin C. In contrast to the placebo group, those given vitamin C experienced a decrease in depression scores and also greater FSI. What is FSI? Frequency of Sexual Intercourse.

Evidently, high dose vitamin C improves mood and intercourse frequency, but only in sexual partners that don't live with one another. In the placebo group, those not living together had sex about once a week, and those living together a little higher, once every five days, with no big change on vitamin C. But for those not living together, on vitamin C? Every other day! The differential effect for non-cohabitants suggests that the mechanism is not a peripheral one, meaning outside the brain, but a central one--some psychological change which motivates the person to venture forth to have intercourse. The mild antidepressant effect they found was unrelated to cohabitation or frequency, so it does not appear that the depression scores improved just because of the improved FSI.

According to the Centers for Disease Control and Prevention, the rates of all of our top 10 killers have fallen or stabilized except for one, suicide. As shown in my video, Antioxidants & Depression, accumulating evidence indicates that free radicals may play important roles in the development of various neuropsychiatric disorders including major depression, a common cause of suicide.

In a study of nearly 300,000 Canadians, for example, greater fruit and vegetable consumption was associated with lower odds of depression, psychological distress, self-reported mood and anxiety disorders and poor perceived mental health. They conclude that since a healthy diet comprised of a high intake of fruits and vegetables is rich in anti-oxidants, it may consequently dampen the detrimental effects of oxidative stress on mental health.

But that study was based on asking how many fruits and veggies people ate. Maybe people were just telling the researchers what they thought they wanted to hear. What if you actually measure the levels of carotenoid phytonutrients in people's bloodstreams? The same relationship is found. Testing nearly 2000 people across the United States, researchers found that a higher total blood carotenoid level was indeed associated with a lower likelihood of elevated depressive symptoms, and there appeared to be a dose-response relationship, meaning the higher the levels, the better people felt.

Lycopene, the red pigment predominantly found in tomatoes (but also present in watermelon, pink grapefruit, guava and papaya) is the most powerful carotenoid antioxidant. In a test tube, it's about 100 times more effective at quenching free radicals than a more familiar antioxidant like vitamin E.

Do people who eat more tomatoes have less depression, then? Apparently so. A study of about a thousand older men and women found that those who ate the most tomato products had only about half the odds of depression. The researchers conclude that a tomato-rich diet may have a beneficial effect on the prevention of depressive symptoms.

Higher consumption of fruits and vegetables has been found to lead to a lower risk of developing depression, but if it's the antioxidants can't we just take an antioxidant pill? No.

Only food sources of antioxidants were protectively associated with depression. Not antioxidants from dietary supplements. Although plant foods and food-derived phytochemicals have been associated with health benefits, antioxidants from dietary supplements appear to be less beneficial and may, in fact, be detrimental to health. This may indicate that the form and delivery of the antioxidants are important. Alternatively, the observed associations may be due not to antioxidants but rather to other dietary factors, such as folate, that also occur in plant-rich diets.

In a study of thousands of middle-aged office workers, eating lots of processed food was found to be a risk factor for at least mild to moderate depression five years later, whereas a whole food pattern was found to be protective. Yes, it could be because of the high content of antioxidants in fruits and vegetables but could also be the folate in greens and beans, as some studies have suggested an increased risk of depression in folks who may not have been eating enough.

Low folate levels in the blood are associated with depression, but since most of the early studies were cross-sectional, meaning a snapshot in time, we didn't know if the low folate led to depression or the depression led to low folate. Maybe when you have the blues you don't want to eat the greens.

But since then a number of cohort studies were published, following people over time. They show that a low dietary intake of folate may indeed be a risk factor for severe depression, as much as a threefold higher risk. Note this is for dietary folate intake, not folic acid supplements; those with higher levels were actually eating healthy foods. If you give people folic acid pills they don't seem to work. This may be because folate is found in dark green leafy vegetables like spinach, whereas folic acid is the oxidized synthetic compound used in food fortification and dietary supplements because it's more shelf-stable. It may have different effects on the body as I previously explored in Can Folic Acid Be Harmful?

These kinds of findings point to the importance of antioxidant food sources rather than dietary supplements. But there was an interesting study giving people high dose vitamin C. In contrast to the placebo group, those given vitamin C experienced a decrease in depression scores and also greater FSI. What is FSI? Frequency of Sexual Intercourse.

Evidently, high dose vitamin C improves mood and intercourse frequency, but only in sexual partners that don't live with one another. In the placebo group, those not living together had sex about once a week, and those living together a little higher, once every five days, with no big change on vitamin C. But for those not living together, on vitamin C? Every other day! The differential effect for non-cohabitants suggests that the mechanism is not a peripheral one, meaning outside the brain, but a central one--some psychological change which motivates the person to venture forth to have intercourse. The mild antidepressant effect they found was unrelated to cohabitation or frequency, so it does not appear that the depression scores improved just because of the improved FSI.

Vegetarians and vegans are all too familiar with the question: Where do you get your protein?

Well, we can finally put to rest the question of whether vegetarians get enough protein thanks to a large study that compared the nutrient profiles of about 30,000 non-vegetarians to 20,000 vegetarians and about 5,000 vegans, 5,000 flexitarians (vegetarian most of the time), and 5,000 pescetarians (no meat except fish). The average requirement is 42 grams of protein a day. As you can see in the graph in the video, Do Vegetarians Get Enough Protein, meat eaters get way more than they need, and so does everyone else. Vegetarians and vegans average 70% more protein than the recommendation every day.

It's surprising that there's so much fuss about protein in this country when less than 3% of adults don't make the cut, presumably because they're on extreme calorie-restricted diets and aren't eating enough food period. But 97% of Americans get enough protein.

There is a nutrient, though, for which 97% of Americans are deficient. That nutrient is fiber.

Less than 3% of Americans get even the recommended minimum adequate intake of fiber. That's something we really have to work on.

On average, we get only about 15 grams a day. The minimum daily requirement is 31.5, so we get less than half the minimum. Men are particularly deficient. If we break down intake by age and gender, after studying the diets of 12,761 Americans, the percent of men between ages 14 and 50 getting the minimum adequate intake is zero. (The only nutrient Americans may be more deficient in than fiber is potassium. See 98% of American Diets Potassium Deficient.)

This deficit is stunning in that dietary fiber has been protectively associated in population studies with the risk of diabetes, metabolic syndrome, cardiovascular disease, obesity, and various cancers as well high cholesterol, blood pressure, and blood sugars. Therefore, it is not surprising that fiber is listed as a nutrient of concern reported by the Dietary Guidelines Advisory Committee. Protein is not.

One problem is that most people have no idea what's in their food; more than half of Americans think steak is a significant fiber source. By definition, fiber is only found in plants. There is no fiber in meat, dairy or eggs, and little or no fiber in junk food. Therein lies the problem. Americans should be eating more beans, vegetables, fruits, and whole grains--but how are they doing?

Even semi-vegetarians make the fiber minimum, though. Those eating completely plant-based diets triple the average American intake. When closing the fiber gap, you'll want to do it gradually though, no more than about five extra grams a day each week until you can work your way up. But it's worth it. "Plant-derived diets tend to contribute significantly less fat, saturated fat, cholesterol, and food-borne pathogens, while at the same time offering more fiber, folate, vitamin C, and phytochemicals, all essential factors for disease prevention, optimal health, and well being." And the more whole plant foods the better. If we compare the nutritional quality of vegan versus vegetarian, semi-vegetarian, pesco-vegetarian and omnivorous diets, traditional healthy diet indexing systems consistently indicate that the most plant-based diet is the healthiest one.

Beans are an essential part of any healthful diet. The federal government recommends about half a cup a day of beans, counting them as both a protein and a vegetable since they have the best of both worlds. Beans are excellent sources of fiber, folate, plant protein, plant iron, vitamin B1, and minerals such as magnesium, phosphorus, potassium, and copper, all while being naturally low in sodium.

Yet Americans don't know beans! 96% of Americans don't even meet the measly minimum recommended intake of beans, chickpeas, split peas or lentils. The same percentage of Americans don't eat their greens every day. Two of the healthiest foods on the planet are greens and beans, but hardly anyone even consumes the minimum recommended amount. As a team of researchers from the National Cancer Institute noted, this is just another "piece added to the rather disturbing picture that is emerging of a nation's diet in crisis."

But how should we get our beans? Canned beans are convenient, but are they as nutritious as home-cooked? And if we do used canned, should we drain them or not? A recent study published in Food and Nutrition Sciences spilled the beans.

In addition to their health benefits, beans are cheap. The researchers did a little bean counting, and a serving of beans costs between ten cents and, if we want to go crazy, 40 cents.

The researchers compiled a table, which you can see in my video, Canned Beans or Cooked Beans?, of the cost per serving of beans, both canned and cooked. Canned beans cost about three times more than dried beans, but dried beans can take hours to cook, so my family splurges on canned beans, paying the extra 20 cents a serving. Nutrition-wise, cooked and canned are about the same, but the sodium content of canned beans can be 100 times that of cooked. Draining and rinsing the canned beans can get rid of about half the sodium, but you're also draining and rinsing away some of the nutrition. I recommend, when buying canned beans, to instead get the no-salt added varieties, and to keep and use the bean juice.

The bottom line is that beans, regardless of type or form, are a nutrient rich food and should be encouraged as part of an overall healthy diet.

We know that vegetarians tend to be slimmer, but there's a perception that veg diets may somehow be deficient in nutrients. So how's this for a simple study, profiled in my video Nutrient-Dense Approach to Weight Management: an analysis of the diets of 13,000 people, comparing the nutrient intake of those eating meat to those eating meat-free.

They found that those eating vegetarian were getting higher intakes of nearly every nutrient: more fiber, more vitamin A, more vitamin C, more vitamin E, more of the B vitamins (thiamin, riboflavin, & folate), more calcium, more magnesium, more iron, and more potassium. At the same time, they were also eating less of the harmful stuff like saturated fat and cholesterol. And yes, they got enough protein.

And some of those nutrients are the ones Americans really struggle to get enough of--like fiber, vitamins A, C, and E, calcium, magnesium, potassium--and those eating vegetarian got more of all of them. Even so, just because they did better than the standard American diet isn't saying much--they still didn't get as much as they should have. Those eating vegetarian ate significantly more dark green leafy vegetables, but that comes out to just two more teaspoons of greens than meat eaters on average every day.

In terms of weight management, the vegetarians were consuming, on average, 363 fewer calories every day. That's what people do when they go on a diet and restrict their food intake--but it seemed like that is how vegetarians just ate normally.

How sustainable are more plant-based diets long term? They are among the only type of diet that has been shown to be sustainable long-term, perhaps because not only do people lose weight but they often feel so much better.

And there's no calorie counting or portion control. In fact, vegetarians may burn more calories in their sleep. Those eating more plant-based diets appear to have an 11% higher resting metabolic rate. Both vegetarians and vegans seem to have a naturally revved up metabolism compared to those eating meat.

Having said that, the vegetarians in the first study mentioned were also eating eggs and dairy, so while they were significantly slimmer than those eating meat, they were still, on average, overweight. As profiled in my video, Thousands of Vegans Studied, the only dietary pattern associated on average with an ideal body weight was a strictly plant-based one. But at least the study helps to dispel the myth that meat-free diets are somehow nutrient-deficient. In fact, the editor-in-chief of the Journal of the American Dietetic Associationasked, "What could be more nutrient dense than a vegetarian diet?"

Anyone can lose weight in the short term on nearly any diet, but diets don't seem to work in the long-term. That's because we don't need a "diet"; we need a new way of eating that we can comfortably stick with throughout our lives. If that's the case, then we better choose to eat in a way that will most healthfully sustain us. That's why a plant-based diet may offer the best of both worlds. It's the only diet, for example, shown to reverse heart disease-our number one killer-in the majority of patients, as described in my video: One in a Thousand: Ending the Heart Disease Epidemic.

There are a number of theories offered as to why those eating plant-based are, on average, so much slimmer. Check out these videos for more information:

I previously lampooned the egg industry PR campaign that tried to promote eggs as a source of eyesight-saving nutrients such as lutein, by noting that a single spoonful of spinach had as much as nine eggs (see Egg Industry Blind Spot). The reason we'll only hear that egg industry claim on websites and TV shows, and never in an ad or on an egg carton, is because there are laws against false and misleading advertising that don't allow the industry to say eggs contain lutein because there's such an insignificant amount.

In an email I retrieved through the Freedom of Information Act (you can see the email in my video Eggs and Choline: Something Fishy), the head of the USDA's poultry research and promotion programs reminded the egg industry that they can't mention lutein in an egg ad. They can't say it helps people with macular degeneration, and can't even talk about how good lutein is for us since "eggs have such a wee amount, and given eggs' fat and cholesterol content this is a nonstarter for anything but PR." So for public relations, companies can lie through your teeth, but there are laws covering truthfulness in ads.

The industry can't say eggs are a source of omega 3s, iron, or folate either. They can't even honestly call eggs a rich source of protein. The USDA Agriculture Marketing Service suggested that the egg industry instead boast about the choline content of eggs, one of only two nutrients that eggs are actually rich in, besides cholesterol.

So the egg industry switched gears. A priority objective of the American Egg Board became "to make choline out to be an urgent problem and eggs the solution." They outlined how they could partner with a physician's group and write an "advertorial." They developed a number of them for nutrition journals. An advertorial is an advertisement parading as an objective editorial. They sent letters out to doctors arguing that "inadequate intake of choline has tremendous public health implications." So forget about the cholesterol--the "elephant-in-the-room," as the industry calls it--and focus on this conjured epidemic of choline deficiency.

People actually get about twice the choline they need and, in fact, too much choline can be the real problem. For one thing, too much choline can give breath, urine, sweat, saliva, and vaginal secretions an odor resembling rotten fish. Millions of Americans have a genetic defect that causes a fishy body odor and might benefit from a low-choline diet, since choline is converted in our gut into the fishy compound trimethylamine (TMA). Individuals oozing trimethylamine often become vegans because reducing the ingestion of dietary animal products rich in lipids decreases TMA production and the associated noxious odor. The other 99 percent of us, though, can turn the fishy choline compound into trimethylamine oxide, which is 100 times less stinky. We used to think extra choline was harmless for the 99 percent, but not anymore.

Researchers at the Cleveland Clinic found that dietary choline (after it is converted in our gut to trimethylamine and oxidized in our liver to form trimethylamine oxide) may contribute to plaque build-up in people's arteries. This may set us up for heart disease, stroke, and death. Which foods is choline predominantly found in? Eggs, milk, liver, red meat, poultry and fish.

The good news is that this may mean a new approach to prevent or treat heart disease, the most obvious of which would be to limit dietary choline intake. But if that means decreasing egg, meat and dairy consumption, then the new approach sounds an awful lot like the old approach - adopting a plant-based diet.

Choline may be one of the reasons people following the Atkins diet are at increased risk of heart disease whereas a more plant-based diet like Ornish's can instead reverse our number one killer (see Low Carb Diets and Coronary Blood Flow). This new research adds choline to the list of dietary culprits with the potential to increase the risk of heart disease, making eggs a double whammy--the most concentrated common source of both choline and cholesterol.

The number one question in sleep research is “Why do we sleep?” followed by the question,“How much sleep do we need?” After literally hundreds of studies, we still don’t know the best answer to either question. A few years ago, I featured a large, 100,000-person study which suggested that both short and long sleep duration were associated with increased mortality, with people getting around seven hours of sleep living longest (See Optimal Sleep Duration). Since then, a meta-analysis that included over a million people was published, and found the same thing.

We still don’t know, however, whether "sleep duration is a cause or simply a marker of ill health." Maybe sleeping too little or too long does make us unhealthy—or maybe we see the associated shortened lifespan because being unhealthy causes us to sleep shorter or longer.

Similar work has now been published on cognitive function. After controlling for a long list of factors, men and women in their 50s and 60s getting seven or eight hours appeared to have the best short-term memory compared to those that got much more or much less. The same thing was just demonstrated with immune function where “both reduced and prolonged habitual sleep durations were associated with an increased risk of pneumonia.”

It’s easy to not get too much sleep—just set an alarm. But what if we’re having problems getting enough? What if we’re one of the one in three adults that suffer symptoms of insomnia? There are sleeping pills like Valium that we can take in the short term, but they have a number of adverse side effects. Non-pharmacological approaches such as cognitive behavioral therapy are often difficult, time-consuming, and not always effective. Wouldn’t it be great to have “natural treatments that can improve both sleep onset and help patients improve the quality of sleep while improving next-day symptoms over the long term?”

What about a study on kiwifruit, featured in my video, Kiwifruit for Insomnia? Participants were given two kiwifruit an hour before bed every night for four weeks. Why kiwifruits? Well, people with sleep disorders tend to have high levels of oxidative stress, so maybe antioxidant rich foods might help? But all fruits and vegetables have antioxidants. Kiwifruits contain twice the serotonin of tomatoes—but it shouldn’t cross the blood-brain barrier. Kiwifruit has folate, and a deficiency might cause insomnia—but there’s a lot more folate in some other plant foods.

The reason they studied kiwifruits is because they got grant money from a kiwifruit company. And I’m glad they did because they found some really remarkable results: significantly improved sleep onset, duration, and efficiency using both subjective and objective measurements. Participants went from sleeping an average of six hours a night to seven—by just eating a few kiwifruits.

The number one question in sleep research is “Why do we sleep?” followed by the question,“How much sleep do we need?” After literally hundreds of studies, we still don’t know the best answer to either question. A few years ago, I featured a large, 100,000-person study which suggested that both short and long sleep duration were associated with increased mortality, with people getting around seven hours of sleep living longest (See Optimal Sleep Duration). Since then, a meta-analysis that included over a million people was published, and found the same thing.

We still don’t know, however, whether "sleep duration is a cause or simply a marker of ill health." Maybe sleeping too little or too long does make us unhealthy—or maybe we see the associated shortened lifespan because being unhealthy causes us to sleep shorter or longer.

Similar work has now been published on cognitive function. After controlling for a long list of factors, men and women in their 50s and 60s getting seven or eight hours appeared to have the best short-term memory compared to those that got much more or much less. The same thing was just demonstrated with immune function where “both reduced and prolonged habitual sleep durations were associated with an increased risk of pneumonia.”

It’s easy to not get too much sleep—just set an alarm. But what if we’re having problems getting enough? What if we’re one of the one in three adults that suffer symptoms of insomnia? There are sleeping pills like Valium that we can take in the short term, but they have a number of adverse side effects. Non-pharmacological approaches such as cognitive behavioral therapy are often difficult, time-consuming, and not always effective. Wouldn’t it be great to have “natural treatments that can improve both sleep onset and help patients improve the quality of sleep while improving next-day symptoms over the long term?”

What about a study on kiwifruit, featured in my video, Kiwifruit for Insomnia? Participants were given two kiwifruit an hour before bed every night for four weeks. Why kiwifruits? Well, people with sleep disorders tend to have high levels of oxidative stress, so maybe antioxidant rich foods might help? But all fruits and vegetables have antioxidants. Kiwifruits contain twice the serotonin of tomatoes—but it shouldn’t cross the blood-brain barrier. Kiwifruit has folate, and a deficiency might cause insomnia—but there’s a lot more folate in some other plant foods.

The reason they studied kiwifruits is because they got grant money from a kiwifruit company. And I’m glad they did because they found some really remarkable results: significantly improved sleep onset, duration, and efficiency using both subjective and objective measurements. Participants went from sleeping an average of six hours a night to seven—by just eating a few kiwifruits.